The New York University Head Injury Clinical Center will continue to be concerned with detailed characterization of the manner in which cerebral blood flow (CBF), cerebral oxidative metabolism (CMRO2) and pulmonary function fail after severe human head injury, a major cause in the United States of neurological morbidity and mortality. Mass spectrometric studies of CBF and CMRO2 in acute human head injury will be continued to determine the prognostic value of CMRO2 acutely with respect to its established value several days after injury. Parallel serial observations of motor, speech, oculocephalic, oculovestibular, and respiratory responses as well as somatosensory, auditory, and visual evoked responses after head injury will be made to construct a prognostic profile. A rat model of altered states of consciousness after brain stem lesions will be studied to determine the time course of development of changes in cerebral intracellular metabolites including: adenosine nucleotides, creatine phosphate and glycolytic and citric acid cycle intermediates; and parallel changes in regional cerebral blood flow, regional glucose metabolism, oxidative metabolism, and brain microscopic morphology to define the pathophysiologic basis for these changes. Rat model data and experimental head trauma data from a cat model of white matter changes after hypoxia, hypotension, and experimental head trauma will be related to clinical and neuropathological observations, particularly of brain edema and ischemia, in order to provide a basis for a rational treatment program for human head injuries. BIBLIOGRAPHIC REFERENCES: Hawkins R, Hass WK, Dorogi P, Ransohoff J: Regional Cerebral Metabolic Rate of Glucose in Rats With Brain Stem Lesions. Stroke 7:5, 1976. Hass WK, Rappaport ZH, Kobayashi M, Dorogi P, Hochwald GM, Ransohoff J: Temporal Effects of Reticular Formation Lesions on Rat Regional Cerebral Blood Flow. Stroke 7:7, 1976.